Instructions for use Irbetan-N tablets 300 mg + 12.5 mg blister No. 30
Composition
active ingredients: irbesartan, hydrochlorothiazide;
1 tablet contains irbesartan 150 mg and hydrochlorothiazide 12.5 mg;
Excipients: lactose monohydrate; microcrystalline cellulose; croscarmellose sodium;
pregelatinized starch; magnesium stearate; colloidal anhydrous silica; red iron oxide (E 172); yellow iron oxide (E 172)
or
1 tablet contains irbesartan 300 mg and hydrochlorothiazide 12.5 mg;
Excipients: lactose monohydrate; microcrystalline cellulose; croscarmellose sodium;
pregelatinized starch; magnesium stearate; colloidal anhydrous silica; red iron oxide (E 172); yellow iron oxide (E 172).
Dosage form
Pills.
Main physicochemical properties: round tablets with a biconvex surface of orange-pink color with white inclusions. The presence of dark color dye inclusions is allowed.
Pharmacotherapeutic group
Combined preparations of angiotensin-II inhibitors. ATX code C09D A04.
Pharmacological properties
Pharmacodynamics.
Irbetan-H is a combination of the angiotensin-II receptor antagonist irbesartan and the thiazide diuretic hydrochlorothiazide. The combination of these components exhibits an additive antihypertensive effect, in which blood pressure is reduced significantly more than when either component is used alone.
Irbesartan is a potent, orally active, selective angiotensin II receptor (AT1 subtype) antagonist. It can block all actions of angiotensin II mediated by the AT1 receptor, regardless of the source or route of synthesis of angiotensin II. Selective antagonism of angiotensin II (AT1) receptors results in increases in renin and plasma angiotensin II levels and decreases in plasma aldosterone concentrations. In particular, irbesartan, when used at recommended doses in patients not at risk of electrolyte imbalance, has no significant effect on serum potassium. Irbesartan does not inhibit ACE (kininase II), the enzyme that generates angiotensin II, and also degrades bradykinin to inactive metabolites. Irbesartan does not require metabolic activation. Hydrochlorothiazide is a thiazide diuretic. The mechanism of the antihypertensive effect of thiazide diuretics is not fully understood at this time. Thiazides affect the reabsorption of electrolytes in the renal tubules, directly increasing the excretion of sodium and chloride in approximately equal amounts. Due to the diuretic effect of hydrochlorothiazide, plasma volume decreases, plasma renin activity increases, aldosterone secretion increases, as a result of which the loss of potassium and bicarbonate with urine increases and the concentration of potassium in the blood serum decreases. Presumably, due to the blockade of the renin-angiotensin-aldosterone system (RAAS), there is a tendency to compensate for the loss of potassium when irbesartan is used simultaneously. When using hydrochlorothiazide, diuresis begins after 2 hours, and the peak effect occurs at approximately 4 hours, while its effect lasts for approximately 6-12 hours.
The combination of hydrochlorothiazide and irbesartan produces a dose-dependent additional reduction in blood pressure within the therapeutic dose range. The addition of 12.5 mg of hydrochlorothiazide to 300 mg of irbesartan once daily in patients inadequately controlled on 300 mg of irbesartan alone resulted in a placebo-adjusted reduction in diastolic blood pressure to a trough value (24 hours after dosing) of 6.1 mm Hg. The combination of 300 mg of irbesartan and 12.5 mg of hydrochlorothiazide resulted in an overall reduction in systolic/diastolic blood pressure of 13.6/11.5 mm Hg. excluding placebo.
The use of 150 mg of irbesartan and 12.5 mg of hydrochlorothiazide once daily resulted in a reduction in mean systolic/diastolic blood pressure with placebo correction to 12.9/6.9 mm Hg (24 hours after administration) in patients with mild to moderate hypertension. The peak effect was observed after 3-6 hours. When assessed by ambulatory blood pressure monitoring, the combination of 150 mg of irbesartan and 12.5 mg of hydrochlorothiazide once daily resulted in a consistent reduction in blood pressure over 24 hours with a mean reduction in systolic/diastolic blood pressure over 24 hours, excluding placebo, of 15.8/10.0 mm Hg.
The effect of the combination of irbesartan and hydrochlorothiazide on morbidity and mortality has not been studied. Epidemiological studies have shown that long-term treatment with hydrochlorothiazide reduces the risk of cardiovascular morbidity and mortality.
The efficacy of the drug does not depend on the age or sex of the patient. In patients of the black race with arterial hypertension, the response to monotherapy with irbesartan, as well as other drugs that affect the renin-angiotensin system (RAS), is significantly lower. When irbesartan is used simultaneously with a low dose of hydrochlorothiazide (for example, 12.5 mg per day), the antihypertensive response in patients of the black race approaches that of representatives of other races.
Pharmacokinetics.
Concomitant use of hydrochlorothiazide and irbesartan does not affect the pharmacokinetics of either component of the drug.
Irbesartan and hydrochlorothiazide are orally active drugs and do not require biological transformation to be active. After oral administration, the absolute oral bioavailability is 60-80% and 50-80%, respectively, for irbesartan and hydrochlorothiazide. Food does not affect the bioavailability of the drug. Peak plasma concentrations are reached 1.5-2 hours after oral administration for irbesartan and 1-2.5 hours for hydrochlorothiazide.
Irbesartan is approximately 96% bound to plasma proteins, with negligible binding to cellular components of the blood. The volume of distribution of irbesartan is 53-93 liters. Hydrochlorothiazide is 68% bound to plasma proteins, and its confirmed volume of distribution is 0.83-1.14 l/kg.
Irbesartan exhibits linear and dose-proportional pharmacokinetics over the dose range of 10 to 600 mg. Increased absorption has been observed at doses below 600 mg; the mechanism is not clear. Total renal clearance is 157-176 and 3.0-3.5 ml/min, respectively. The terminal half-life of irbesartan is 11-15 hours. Steady-state plasma concentrations are reached within 3 days of starting a once-daily dosing regimen. Limited accumulation of irbesartan (<20%) is observed in plasma after repeated daily dosing. In a study, slightly higher plasma concentrations of irbesartan were observed in female hypertensive patients. However, no difference in half-life and accumulation of irbesartan was found. The dosage of the drug does not require adjustment based on age or gender. The AUC and Cmax values for irbesartan were also slightly higher in elderly patients (≥ 65 years) than in young patients (18-40 years). However, the terminal half-life was not significantly different. No dose adjustment is required for elderly patients. The mean plasma half-life of hydrochlorothiazide has been reported to be 5-15 hours.
After oral administration, the amount of unchanged irbesartan in plasma is 80-85%, as determined by 14C. Irbesartan is metabolized in the liver by glucuronide conjugation and oxidation. The main circulating metabolite is irbesartan glucuronide (approximately 6%). In vitro studies show that irbesartan is primarily oxidized by the cytochrome P450 enzyme CYP2C9; the CYP3A4 isoenzyme has a negligible effect. Irbesartan and its metabolites are excreted both via the liver and the kidneys. After both oral and intravenous administration of 14C-irbesartan, approximately 20% of the radioactivity is excreted in the urine, the remainder in the feces. Less than 2% of the dose is excreted in the urine as unchanged irbesartan. Hydrochlorothiazide is not metabolized but is rapidly excreted by the kidneys. At least 61% of an oral dose is excreted unchanged within 24 hours. Hydrochlorothiazide crosses the placental barrier, but does not cross the blood-brain barrier, and is excreted in breast milk.
Renal impairment: The pharmacokinetics of irbesartan are not significantly altered in patients with renal impairment or in patients undergoing haemodialysis. Irbesartan is not removed by haemodialysis. The half-life of hydrochlorothiazide has been reported to be increased to 21 hours in patients with creatinine clearance < 20 ml/min.
Hepatic impairment: In patients with mild to moderate cirrhosis, the pharmacokinetics of irbesartan are not significantly altered. Studies in patients with severe hepatic impairment have not been conducted.
Indication
Treatment of essential hypertension.
This fixed-dose combination is indicated in adult patients whose blood pressure is not adequately controlled with irbesartan or hydrochlorothiazide alone.
Contraindication
– Hypersensitivity to the components of the drug or to sulfonamide derivatives (hydrochlorothiazide is a sulfonamide derivative).
– Severe renal failure (creatinine clearance < 30 ml/min).
– Persistent form of hypokalemia, hypercalcemia.
– Concomitant use of Irbetan-N with aliskiren-containing drugs in patients with diabetes and patients with moderate to severe renal impairment (glomerular filtration rate < 60 ml/min/1.73 m2).
– Concomitant use of Irbetan-N with angiotensin-converting enzyme (ACE) inhibitors in patients with diabetic nephropathy.
– Treatment-resistant hypokalemia or hypercalcemia.
– Refractory hyponatremia.
– Symptomatic hyperuricemia (gout).
– Anuria.
– Pregnancy or breastfeeding.
– Childhood.
Interaction with other medicinal products and other types of interactions
Other antihypertensive agents. The antihypertensive effect of Irbesartan-N may be enhanced by concomitant administration of other antihypertensive agents. Irbesartan and hydrochlorothiazide (in doses up to 300 mg irbesartan/25 mg hydrochlorothiazide) have been safely administered with other antihypertensive agents, including calcium channel blockers and beta-blockers. Previous treatment with high doses of diuretics may result in volume depletion and a risk of hypotension when irbesartan is started with thiazide diuretics unless volume depletion has been corrected beforehand.
Aliskiren-containing drugs. The simultaneous use of Irbetan-N with aliskiren-containing drugs is contraindicated in patients with diabetes and patients with moderate to severe renal impairment (glomerular filtration rate less than 60 ml/min/1.73 m2) and is not recommended for all other patients.
Lithium preparations. Transient increases in serum lithium concentrations and toxicity have been reported during concomitant use of lithium with ACE inhibitors. Very rare cases of similar effects have been reported with irbesartan. In addition, thiazides reduce the renal excretion of lithium, so the risk of lithium toxicity may increase with the use of this drug. Therefore, the combination of lithium and Irbetan-N is not recommended. If such a combination proves necessary, careful monitoring of serum lithium levels is recommended.
Potassium-sparing medicinal products. The potassium-sparing effect of hydrochlorothiazide is attenuated by the potassium-sparing effect of irbesartan. However, it is believed that this effect of hydrochlorothiazide on serum potassium is possible due to other medicinal products associated with potassium loss and hypokalaemia (e.g. other potassium-sparing diuretics, laxatives, amphotericin, carbenoxolone, penicillin G sodium). Conversely, based on experience with other medicinal products that suppress RAS, the concomitant use of non-potassium-sparing diuretics, potassium-sparing supplements, potassium-containing salt substitutes or other medicinal products that may increase serum potassium (e.g. heparin sodium) may lead to increases in serum potassium. Appropriate monitoring of serum potassium levels is recommended in patients at risk.
Medicinal products affected by serum potassium disturbances. Periodic monitoring of serum potassium is recommended if the drug is used concomitantly with medicinal products whose toxicity is increased by serum potassium disturbances (e.g. digitalis glycosides, antiarrhythmics).
Angiotensin-converting enzyme (ACE) inhibitors. Concomitant use of Irbetan-N with ACE inhibitors is contraindicated in patients with diabetic nephropathy and is not recommended for all other patients.
Non-steroidal anti-inflammatory drugs (NSAIDs): When angiotensin II antagonists are used concomitantly with NSAIDs (i.e. selective COX-2 inhibitors, acetylsalicylic acid (> 3 g/day) and non-selective NSAIDs), attenuation of the antihypertensive effect may occur.
As with ACE inhibitors, concomitant use of angiotensin II antagonists and NSAIDs may lead to an increased risk of worsening of renal function, including possible acute renal failure and increases in serum potassium, especially in patients with pre-existing poor renal function. The combination should be used with caution, especially in elderly patients. Patients should be adequately hydrated and renal function should be monitored after initiation of such combination therapy and during treatment.
Potassium supplements and potassium-sparing diuretics: Based on experience with other medicinal products that affect the renin-angiotensin system (RAS), the concomitant use of potassium-sparing diuretics, potassium supplements, potassium-containing salt substitutes or other medicinal products that may increase serum potassium levels (e.g. heparin) may lead to increases in serum potassium levels and is therefore not recommended.
Additional information on hydrochlorothiazide interactions: When used concomitantly with thiazide diuretics, interactions with the following drugs are possible:
Alcohol: may cause orthostatic hypotension.
Antidiabetic drugs (oral agents and insulins): Dose adjustment of the antidiabetic drug may be required.
Metformin should be used with caution due to the risk of lactic acidosis due to possible hydrochlorothiazide-induced functional renal failure.
Cholestyramine and colestipol resins: in the presence of anion exchange resins, the absorption of hydrochlorothiazide is impaired. The drug Irbetan-N should be taken at least 1 hour before or 4 hours after taking these drugs.
Corticosteroids, adrenocorticotropic hormone (ACTH): electrolyte depletion, especially hypokalemia may be exacerbated.
Digitalis glycosides: Thiazide-induced hypokalemia or hypomagnesemia contributes to the development of digitalis glycoside-induced cardiac arrhythmias.
Nonsteroidal anti-inflammatory drugs: the use of NSAIDs may reduce the diuretic, natriuretic and antihypertensive effects of thiazide diuretics in some patients.
Pressor amines (e.g., norepinephrine): The effect of pressor amines may be reduced, but not enough to preclude their use.
Non-depolarizing muscle relaxants (e.g. tubocurarine): the effect of non-depolarizing muscle relaxants may be potentiated by hydrochlorothiazide.
Gout medications: Dose adjustment of anti-gout medications may be necessary since hydrochlorothiazide may increase serum uric acid levels. Dose increase of probenecid or sulfinpyrazone may be necessary. Concomitant use of thiazide diuretics may increase the incidence of hypersensitivity reactions to allopurinol.
Calcium salts: Thiazide diuretics may increase serum calcium levels due to decreased excretion. If additional calcium-containing drugs or drugs that do not excrete calcium (e.g. vitamin D therapy) are required, serum calcium levels should be monitored and calcium dosage adjusted accordingly.
Carbamazepine: Concomitant use of carbamazepine and hydrochlorothiazide has been associated with a risk of symptomatic hyponatremia. Electrolyte levels should be monitored when these drugs are used concomitantly. If possible, a different class of diuretic should be used.
Drugs whose effects are affected by changes in serum potassium levels.
Periodic monitoring of serum potassium and ECG is recommended when hydrochlorothiazide is administered concomitantly with drugs whose effects are affected by changes in serum potassium (such as digitalis glycosides and antiarrhythmic drugs) and the following drugs that induce torsades de pointes (including some antiarrhythmic drugs), as hypokalemia is a contributing factor to the development of torsades de pointes:
– class Ia antiarrhythmics (e.g. quinidine, hydroquinidine, disopyramide);
– class III antiarrhythmics (e.g. amiodarone, sotalol, dofetilide, ibutilide);
– some neuroleptics (e.g. thioridazine, chlorpromazine, levomepromazine, trifluoroperazine, cyamemazine, sulpiride, sultopride, amisulpiride, tiapride, pimozide, haloperidol, droperidol);
– other medicines (e.g. bepridil, cisapride, diphemanil, erythromycin for intravenous administration, halofantrine, mizolastine, pentamidine, terfenadine, vincamine for intravenous administration).
Methyldopa: Isolated cases of hemolytic anemia have been reported with concomitant use of hydrochlorothiazide and methyldopa.
Salicylates: When using high doses of salicylates, hydrochlorothiazide may enhance their toxic effects on the central nervous system.
Cyclosporine: Concomitant use of cyclosporine may exacerbate hyperuricemia and increase the risk of gout-like complications.
Alcohol, barbiturates, narcotics, or antidepressants. May increase orthostatic hypotension.
Beta-blockers and diaxozide. Concomitant use of thiazide diuretics, including hydrochlorothiazide, with β-blockers may increase the risk of hyperglycemia. Thiazide diuretics, including hydrochlorothiazide, may potentiate the hyperglycemic effect of diaxozide.
Amantadine: Thiazides, including hydrochlorothiazide, may increase the risk of side effects caused by amantadine.
Specific hyposensitization. ACE inhibition increases the likelihood and severity of anaphylactic and anaphylactoid reactions to insect venom. It is believed that this effect may also be observed for other allergens.
Iodinated contrast media: In the case of diuretic-induced dehydration, the risk of acute renal failure is increased, especially with high doses of iodinated contrast media. Patients should be rehydrated before administration of iodinated contrast media.
Amphotericin B (for parenteral administration), corticosteroids, ACTH and stimulant laxatives. Hydrochlorothiazide increases electrolyte imbalance, mainly hypokalemia.
Other forms of interaction: The hyperglycemic effect of beta-blockers and diazoxide may be potentiated by thiazides.
Anticholinergic agents (e.g. atropine, beperiden) may increase the bioavailability of thiazide-type diuretics by reducing gastrointestinal tone and gastric emptying rate.
Thiazides may increase the risk of adverse effects caused by amantadine. Thiazides may reduce the renal excretion of cytotoxic drugs (e.g. cyclophosphamide, methotrexate) and enhance their suppressive effect on bone marrow function.
Application features
Reduced blood pressure - patients with low blood volume. Irbeta-N is rarely associated with symptomatic reduction in blood pressure in patients with hypertension who do not have other risk factors for low blood pressure. Symptomatic reduction in blood pressure may occur in patients who are volume and/or sodium depleted by intensive diuretic therapy, dietary salt restriction, diarrhea, or vomiting. Such conditions should be corrected before starting treatment with the drug.
Patients with hypertension, type 2 diabetes and chronic kidney disease. The effects of irbesartan on renal and cardiovascular function were not consistent across subgroups analyzed in a study of patients with end-stage chronic kidney disease. In particular, the benefits were less pronounced in women and in non-Caucasian subjects.
Renal artery stenosis – renovascular hypertension. There is an increased risk of severe hypotension and renal failure when patients with bilateral renal artery stenosis or stenosis of the artery to a single functioning kidney are treated with ACE inhibitors or angiotensin II receptor antagonists.
Renal impairment and kidney transplantation. If the drug is used in patients with impaired renal function, periodic monitoring of serum calcium, creatinine and uric acid is recommended. There is no experience in patients who have recently undergone kidney transplantation. Irbeta-N should not be used in patients with severe renal impairment (creatinine clearance < 30 ml/min). Patients with impaired renal function may develop azotemia associated with thiazide diuretics. No dose adjustment is required for patients with renal impairment with creatinine clearance ≥ 30 ml/min. In patients with mild to moderate renal impairment (creatinine clearance ≥ 30 ml/min but < 60 ml/min), this fixed-dose combination should be used with caution.
Dual blockade of the renin-angiotensin-aldosterone system (RAAS). Dual blockade of the RAAS by combining Irbetan-N with aliskiren is not recommended due to the increased risk of hypotension, hyperkalemia, and changes in renal function. The concomitant use of Irbetan-N with aliskiren-containing drugs is contraindicated in patients with diabetes and in patients with moderate to severe renal impairment (glomerular filtration rate < 60 ml/min/1.73 m2).
Hepatic impairment. Thiazides should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor changes in fluid and electrolyte balance may precipitate hepatic coma. There is no clinical experience with the use of Irbetan-N in patients with hepatic impairment.
Thiazides should be used with caution in hepatic disorders and progressive liver disease, as these drugs can cause intrahepatic cholestasis, and even minimal changes in water-salt balance can provoke the development of hepatic coma. Hydrochlorothiazide is contraindicated in patients with severe hepatic insufficiency.
Aortic and mitral valve stenosis, obstructive hypertrophic cardiomyopathy: As with other vasodilators, special precautions are required in patients suffering from aortic or mitral valve stenosis or obstructive hypertrophic cardiomyopathy.
Effects on metabolism and endocrine system. During thiazide diuretic therapy, glucose tolerance may be impaired and signs of latent diabetes mellitus may appear. There is a need to adjust the dosage of insulin or oral hypoglycemic drugs for patients with diabetes.
Elevations in cholesterol and triglyceride levels have been associated with thiazide diuretic therapy; however, minimal or no effect has been reported with the 12.5 mg hydrochlorothiazide dose contained in Irbeta-N.
Some patients receiving thiazide diuretic therapy may develop hyperuricemia or signs of gout.
Electrolyte imbalance: As with any patient taking diuretics, serum electrolyte levels should be monitored periodically at appropriate intervals.
Thiazides, including hydrochlorothiazide, may cause fluid or electrolyte imbalance (hypokalemia, hyponatremia, and hypochloraemic alkalosis). Typical signs of fluid or electrolyte imbalance to look out for include dry mouth, thirst, weakness, fatigue, drowsiness, restlessness, muscle pain or cramps, muscle weakness, decreased blood pressure, oliguria, tachycardia, and gastrointestinal disturbances such as nausea or vomiting.
Although hypokalemia may develop with thiazide diuretics, concomitant therapy with irbesartan may attenuate the hypokalemia that occurs with diuretics. The highest risk of developing hypokalemia is in patients with cirrhosis of the liver, intensive diuresis, in patients who take inadequate amounts of oral electrolytes or are concurrently treated with corticosteroids or ACTH. Conversely, hyperkalemia may occur due to the presence of irbesartan in the composition of the drug Irbetan-N, especially in the presence of renal insufficiency and/or heart failure, as well as diabetes mellitus. Appropriate monitoring of serum potassium is recommended in patients at risk. Caution is required when using diuretics that do not excrete potassium and potassium supplements or salt substitutes containing potassium.
There is no evidence that irbesartan can attenuate or prevent diuretic-induced hyponatremia. Chloride depletion is generally mild and usually does not require treatment.
Thiazides may reduce urinary calcium excretion and cause a transient and minor increase in serum calcium in the absence of known disorders of calcium metabolism. Severe hypercalcemia may indicate latent hyperparathyroidism. Thiazides should be discontinued before parathyroid function tests are performed. Thiazides have been shown to increase urinary magnesium excretion, which may lead to hypomagnesemia.
Lithium preparations. It is not recommended to use lithium and Irbetan-N simultaneously.
Anti-doping control: Hydrochlorothiazide, which is contained in this medicinal product, may give a positive analytical result during anti-doping control.
General precautions: When treating patients whose vascular tone and renal function depend mainly on the activity of the RAAS (e.g. patients with severe congestive heart failure or underlying renal disease, including renal artery stenosis), acute hypotension, azotemia, oliguria or acute renal failure may occur with ACE inhibitors or angiotensin II receptor antagonists that affect this system.
As with any antihypertensive agent, excessive reduction of blood pressure in patients with ischemic cardiopathy or ischemic cardiovascular disease may result in myocardial infarction or stroke. Hypersensitivity reactions to hydrochlorothiazide may occur in patients with or without a history of allergy or bronchial asthma, but are more likely to occur in patients with a history of such conditions. Exacerbation or activation of systemic lupus erythematosus has been reported with thiazide diuretics.
Acute myopia and secondary acute angle-closure glaucoma. Medicinal products containing sulfonamides or their derivatives may cause idiosyncrasies leading to transient myopia and acute angle-closure glaucoma. Hydrochlorothiazide is a sulfonamide derivative, but only isolated cases of acute angle-closure glaucoma have been reported with hydrochlorothiazide. Symptoms of this condition include acute visual impairment or eye pain. These symptoms usually develop within hours to weeks of initiating therapy with this medicinal product. If acute angle-closure glaucoma is left untreated, it may lead to irreversible vision loss in the patient. If such a symptom occurs, the first step should be to discontinue therapy with this medicinal product as soon as possible. If intraocular pressure remains uncontrolled after this, medical or surgical treatment may be considered. Risk factors for developing acute angle-closure glaucoma may include a history of allergy to sulfonamide or penicillin.
Effect of hydrochlorothiazide on laboratory test results:
– the drug may reduce the level of protein-bound iodine in blood plasma;
– treatment with the drug should be discontinued before conducting a laboratory examination to assess parathyroid function;
– the drug is capable of increasing the concentration of free bilirubin in blood serum.
Non-melanoma skin cancer: Results from two recent pharmacoepidemiological studies (based on Danish national data sources, including the Danish Cancer Registry and the National Register of Prescribed Medicines) have shown an overall dose-dependent association between hydrochlorothiazide use and the occurrence of basal cell carcinoma and squamous cell carcinoma.
The photosensitizing effect of hydrochlorothiazide may be the cause of the development of such pathologies. Patients taking hydrochlorothiazide alone or in combination with other drugs should be informed of the risk of non-melanoma skin cancer and advised to regularly examine their skin for new lesions, as well as changes in existing ones, and to report any suspicious skin lesions.
Suspicious skin lesions should be histologically examined by biopsy. Patients should be advised to limit exposure to sunlight and UV rays and to use appropriate protection when exposed to sunlight and UV rays to minimize the risk of skin cancer.
The use of hydrochlorothiazide should also be carefully reconsidered in patients with a history of skin cancer (see section 4.8).
Lactose: This medicinal product contains lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicinal product.
Use during pregnancy or breastfeeding
Pregnancy. The use of the drug is contraindicated during pregnancy. When pregnancy is diagnosed, treatment with ARA II should be stopped immediately and, if necessary, alternative therapy should be started.
Breastfeeding. The use of the drug Irbetan-N is contraindicated during breastfeeding.
Ability to influence reaction speed when driving vehicles or other mechanisms
Studies on the effect on the ability to drive and use machines have not been conducted. Based on the pharmacodynamic properties of the drug, its effect on this ability is unlikely. When driving or operating machinery, it should be taken into account that drowsiness or fatigue may occur during the treatment of arterial hypertension.
Method of administration and doses
The medicine should be taken once a day, regardless of meals.
If clinically appropriate, direct switching from monotherapy to fixed combinations may be considered:
Irbetan-N 150 mg/12.5 mg can be used in patients whose blood pressure is not adequately controlled by hydrochlorothiazide or irbesartan 150 mg alone;
Irbetan-N 300 mg/12.5 mg can be used in patients whose blood pressure is not adequately controlled with irbesartan 300 mg or Irbetan-N 150 mg/12.5 mg.
If necessary, Irbetan-N can be used with other antihypertensive drugs.
